肝纤维化与肝硬化组织中趋化因子CXCL5和CXCL8的表达意义

目的 探讨肝纤维化与肝硬化组织中趋化因子CXCL5和CXCL8的表达意义.方法 收集2008年5月至2009年5月南方医科大学南方医院9例肝血管瘤患者、10例肝纤维化患者和11例肝硬化患者肝组织标本,采用ELISA法检测肝组织中的CXCL5和CXCL8的含量.采用单因素方差分析,双变量正态分布采用Pearson等级相关分析,不符合双变量正态分布的采用Spearman相关系数表示.结果 肝血管瘤、肝纤维化、肝硬化患者肝组织中CXCL5的含量分别为(0.8±0.7)、(2.0±2.0)、(17.1±4.8)ng/g;CXCL8的含量分别为(6.2±3.7)、(11.6±3.5)、(12.3±3.9)ng/g;3者比较差异有统计学意义(F=60.050,7.690,P＜0.05).CXCL5与ALT、AST、PT具有相关性(r=0.502,0.468,0.523,P＜0.05);CXCL8与ALT、AST、TBil、PT具有相关性(r=0.477,0.504,0.537,0.431,P＜0.05).结论 肝脏发生纤维化损伤时CXCL5和CXCL8的含量均显著增高,但两者的变化规律不同.CXCL5和CXCL8的变化与肝脏损伤有关,但变化的程度与肝病的损害程度不完全一致.     

趋化因子CXCL5在前列腺癌中的表达和意义

目的：观察CXC趋化因子配体-5（CXC chemokine Ligand-5,CXCL5）在前列腺癌中的表达,探讨CXCL-5在前列腺癌发生、发展、侵袭及转移中的作用.方法：采用免疫组织化学SP法检测41例前列腺癌、6例PIN、及14例前列腺增生中CXCL5的表达情况,染色后阅片、评分,对比其在各组之间表达的差异,分析其与前列腺癌病理分级、临床分期及肿瘤转移的关系.结果：CXCL5在前列腺癌组中的表达明显高于PIN组和前列腺增牛组,差异有统计学意义（P＜0.01）;在小同病理分级前列腺癌组织中,从高分化组到低分化组CXCL5染色强度逐渐加深,染色评分逐渐升高,差异有统计学意义（P＜0.05）;CXCL5在Whitmore-Jewett分期系统C＋D期组的表达明显高于A＋B期组,差异有统计学意义（P＜0.05）;CXCL5在转移性前列腺癌组中的表达明显高于无转移组,差异有统计学意义（P＜0.05）.结论：CXCL5在前列腺癌组织中的表达高于前列腺增生和PIN,其表达随前列腺癌病理恶性程度、临床分期进展、伴随转移而增强.CXCL5可能参与了前列腺癌的发生、发展与转移过程.     

Chemokines in Vitiligo Pathogenesis: CXCL10 and 12

BackgroundVitiligo is a common pigmentary disease that affects 0.5% to 1% of the global population. The main manifestation of vitiligo is skin depigmentation, which significantly influences appearance and brings enormous psychological stress for patients. C-X-C motif chemokine ligand 9 (CXCL9), CXCL10 , CXCL11 and CXCL12 are linked to the Th1 pattern and have been suggested as one of the most relevant chemokine axes that promote T cell migration in different autoimmune and inflammatory process . These were suggested to promote melanocyte-specific cytotoxic T lymphocyte (CTLs) to infiltrate into the basal layer of the epidermis to attack melanocytes, resulting in the deficiency of melanin.ObjectiveThe aim of this study was to evaluate the role of CXCL10 and CXCL12 in the pathogenesis of vitiligo and to detect its relationship to disease activity.MethodsForty patients with non-segmental vitiligo (NSV; 20 patients with active disease and 20 stable patients). This group included 20 male patients and 20 female patients, with ages ranging from 10 to 65 years. Twenty healthy age- and sex-matched controls were included. The control group included 10 males and 10 females with ages ranging from 10 to 65 years. We measured the serum level of CXCL10 and CXCL12 in the patients and controls using the enzyme-linked immunosorbent assay (ELISA) method.ResultsSerum CXCL10 level was highly significantly increased in patients with vitiligo compared to controls. There was a high statistically significant difference between patients with active disease and those with stable disease regarding serum level of CXCL10 with higher level of CXCL10 in active type.ConclusionOur results suggest that vitiligo might be associated with increased serum levels of CXCL10 and CXCL12. There is a positive relationship to disease activity, indicating that CXCL10 and CXCL12 may play a significant role in the pathogenesis of vitiligo.     

MicroRNA-155 Drives TH17 Immune Response and Tissue Injury in Experimental Crescentic GN

CD4⁺ T cells play a pivotal role in the pathogenesis of autoimmune disease, including human and experimental crescentic GN. Micro-RNAs (miRs) have emerged as important regulators of immune cell development, but the impact of miRs on the regulation of the CD4⁺ T cell immune response remains to be fully clarified. Here, we report that miR-155 expression is upregulated in the kidneys of patients with ANCA-associated crescentic GN and a murine model of crescentic GN (nephrotoxic nephritis). To elucidate the potential role of miR-155 in T cell-mediated inflammation, nephritis was induced in miR-155^−/− and wild-type mice. The systemic and renal nephritogenic T_H17 immune response decreased markedly in nephritic miR-155^−/− mice. Consistent with this finding, miR-155–deficient mice developed less severe nephritis, with reduced histologic and functional injury. Adoptive transfer of miR-155^−/− and wild-type CD4⁺ T cells into nephritic recombination activating gene 1-deficient (Rag-1^−/−) mice showed the T cell-intrinsic importance of miR-155 for the stability of pathogenic T_H17 immunity. These findings indicate that miR-155 drives the T_H17 immune response and tissue injury in experimental crescentic GN and show that miR-155 is a potential therapeutic target in T_H17-mediated diseases.In the last decade, it has become clear that the CD4⁺ T helper cell-driven immune response significantly contributes to renal tissue injury in human and experimental crescentic GN.^1–3 CD4⁺ T cells can be classified according to their cytokine expression profile into four major subsets, namely T_H1, T_H2, T_H17, and regulatory T cells (Tregs).^4–7 Recent studies have highlighted the pivotal pathogenic role of the T_H1 and T_H17 immune responses in crescentic GN,^8,9 including the identification and characterization of IFN-γ– and IL-17A–producing CD4⁺ T cells in nephritic kidneys of mice and humans, as well as evidence for the contribution of IFN-γ and IL-17A/IL-23 to renal tissue injury in GN.^10–13 However, the precise regulation of systemic and renal CD4⁺ T cell immunity in crescentic GN remains to be elucidated.Micro-RNAs (miRNAs) are small, noncoding RNAs that bind to mRNA and mediate mRNA cleavage, translational repression, or mRNA destabilization.¹⁴ miRNAs are essential for animals, and Dicer knockout mice, which are deficient in the enzyme for final miRNA processing, are not viable because of the lack of mature miRNAs.¹⁵ As fine-tuning regulators of gene expression, miRNAs are involved in various cellular processes and have emerged as important regulators of immune cell development. Mice deficient in T cell miRNAs have vital T helper cells with an impaired capacity to proliferate.¹⁶ Moreover, individual miRNAs have been implicated in T cell function, especially in influencing T_H1 cells,¹⁷ T_H17 cells,^18,19 and Treg cells.²⁰ Recently, miRNA-146 (miR-146) and miR-155 have been shown to be increased in both the urine and kidney of patients with IgA nephropathy.²¹ In addition, miR-193a might play a unique role in irreversible podocyte injury in human FSGS²²; however, the functional role of miRNAs in autoimmune-mediated kidney disease is largely unknown.The aim of the present study was to elucidate the role of miRNAs in human and experimental crescentic GN. Therefore, we (1) assessed the expression profile of miRNAs in human and experimental crescentic GN, (2) studied the potential functional role of miRNAs in nephrotoxic nephritis with a specific focus on CD4⁺ T cell immune response, and (3) evaluated the potential mechanisms of miRNA-mediated regulatory processes in murine crescentic GN.     

Characterization of a Factor H Mutation That Perturbs the Alternative Pathway of Complement in a Family with Membranoproliferative GN

Complement C3 activation is a characteristic finding in membranoproliferative GN (MPGN). This activation can be caused by immune complex deposition or an acquired or inherited defect in complement regulation. Deficiency of complement factor H has long been associated with MPGN. More recently, heterozygous genetic variants have been reported in sporadic cases of MPGN, although their functional significance has not been assessed. We describe a family with MPGN and acquired partial lipodystrophy. Although C3 nephritic factor was shown in family members with acquired partial lipodystrophy, it did not segregate with the renal phenotype. Genetic analysis revealed a novel heterozygous mutation in complement factor H (R83S) in addition to known risk polymorphisms carried by individuals with MPGN. Patients with MPGN had normal levels of factor H, and structural analysis of the mutant revealed only subtle alterations. However, functional analysis revealed profoundly reduced C3b binding, cofactor activity, and decay accelerating activity leading to loss of regulation of the alternative pathway. In summary, this family showed a confluence of common and rare functionally significant genetic risk factors causing disease. Data from our analysis of these factors highlight the role of the alternative pathway of complement in MPGN.     

胃癌中 CXCL5表达与临床预后的关系

目的检测趋化因子5(CXCL5)在胃癌中的表达,探讨其表达与病人临床病理特征和生存的关系。方法收集104例胃癌组织标本及其临床病例资料,采用免疫组织化学(IHC)检测胃癌组织中 CXCL5的表达。染色后阅片评分,采用卡方检验、Log-rank、Kaplan-Meier、Cox 回归模型分析 CXCL5的表达与临床病例特征和胃癌病人预后之间的关系。结果IHC 结果显示104例胃癌标本中有45例(43.2%)CXCL5高表达,癌组织中 CXCL5高表达与胃癌病人的 TNM 分期呈正相关(P=0.007),CXCL5高表达组病人预后显著低于其低表达组,5年生存率分别为28.7%和62.8%(P <0.001),Cox 回归模型发现 CXCL5的表达是胃癌病人的独立预后因素之一(HR=2.280,CI：1.301~3.998,P =0.004)。结论CXCL5是影响胃癌病人预后的独立因素,可能与胃癌的进展有关。     

Neutrophil Extracellular Trap-Related Extracellular Histones Cause Vascular Necrosis in Severe GN

Severe GN involves local neutrophil extracellular trap (NET) formation. We hypothesized a local cytotoxic effect of NET-related histone release in necrotizing GN. In vitro, histones from calf thymus or histones released by neutrophils undergoing NETosis killed glomerular endothelial cells, podocytes, and parietal epithelial cells in a dose-dependent manner. Histone-neutralizing agents such as antihistone IgG, activated protein C, or heparin prevented this effect. Histone toxicity on glomeruli ex vivo was Toll-like receptor 2/4 dependent, and lack of TLR2/4 attenuated histone-induced renal thrombotic microangiopathy and glomerular necrosis in mice. Anti–glomerular basement membrane GN involved NET formation and vascular necrosis, whereas blocking NET formation by peptidylarginine inhibition or preemptive anti-histone IgG injection significantly reduced all aspects of GN (i.e., vascular necrosis, podocyte loss, albuminuria, cytokine induction, recruitment or activation of glomerular leukocytes, and glomerular crescent formation). To evaluate histones as a therapeutic target, mice with established GN were treated with three different histone-neutralizing agents. Anti-histone IgG, recombinant activated protein C, and heparin were equally effective in abrogating severe GN, whereas combination therapy had no additive effects. Together, these results indicate that NET-related histone release during GN elicits cytotoxic and immunostimulatory effects. Furthermore, neutralizing extracellular histones is still therapeutic when initiated in established GN.     

趋化因子CXCL5在肝癌中的表达及其临床意义

目的：探讨趋化因子配体5（CXCL5）在原发性肝细胞肝癌（HCC）中的表达,分析其在肝癌发生、发展、侵袭及转移中的作用。 方法：收集218例HCC组织标本及其临床病理资料,采用免疫组化（IHC）Elvision检测肝癌组织、癌旁组织、周围正常组织中CXCL5的表达,染色后阅片、评分、对比其在各组之间的表达差异;采用相关分析、非参数检验、Log-Rank、Cox回归分析和Logistic回归分析进行统计学分析,P 〈 0.05认为有统计学意义。 结果：IHC结果显示CXCL5在癌组织中的阳性率高于癌旁组织（P 〈 0.01）和周围正常组织（P 〈 0.01）;癌组织CXCL5中高表达与门静脉癌栓形成、BCLC分期、TNM分期、肝癌并静脉侵犯正相关,与病理分级负相关;CXCL5是肝癌患者的独立预后因素之一（HR 1.734;P = 0.001）。 结论：CXCL5在HCC中表达增高,与肝癌的病理分级、恶性程度、门静脉癌栓、临床分期呈正相关,其高表达是HCC的独立预后危险因子之一。     

CXCL5 is required for angiogenesis,but not structural adaptation after small bowel resection

Purpose

Intestinal adaptation is the compensatory response to massive small bowel resection (SBR) and characterized by lengthening of villi and deepening of crypts, resulting in increased mucosal surface area. Previous studies have demonstrated increased villus capillary blood vessel density after SBR, suggesting a role for angiogenesis in the development of resection-induced adaptation. Since we have previously shown enhanced expression of the proangiogenic chemokine CXCL5 after SBR, the purpose of this study was to determine the effect of disrupted CXCL5 expression on intestinal adaptation.

Methods

CXCL5 knockout (KO) and C57BL/6 wild type (WT) mice were subjected to either a 50% proximal SBR or sham operation. Ileal tissue was harvested on postoperative day 7. To assess for adaptation, villus height and crypt depth were measured. Submucosal capillary density was measured by CD31 immunohistochemistry.

Results

Both CXCL5-KO and WT mice demonstrated normal structural features of adaptation. Submucosal capillary density increased in the WT but not in the KO mice following SBR.

Conclusion

CXCL5 is required for increased intestinal angiogenesis during resection-induced adaptation. Since adaptive villus growth occurs despite impaired CXCL5 expression and enhanced angiogenesis, this suggests that the growth of new blood vessels is not needed for resection-induced mucosal surface area expansion following massive SBR.     

CXC趋化因子受体5及其配体CXCL13在结直肠癌中的表达及意义

目的 观察CXC趋化因子受体-5(CXCR5)及其特异性配体CXCL13在结直肠癌组织中的表达,探讨其与临床病理特征、预后的关系.方法 用实时定量聚合酶链反应(Real-time PCR)法检测25对结直肠癌及13例结直肠腺瘤冰冻新鲜标本中CXCR5及CXCL13 mRNA的表达,应用免疫组织化学法(IHC)检测153例结直肠癌及相对应的癌旁组织、62例结直肠腺瘤标本中CXCR5及CXCL13蛋白的表达,分析其与临床病理特征、术后生存率的关系.结果 CXCR5及CXCL13mRNA及蛋白表达在结直肠癌组织中的表达率均高于癌旁组织及结直肠腺瘤组织(P均＜0.05).CXCR5与CXCL13的mRNA及蛋白表达呈正相关(PCR:r =0.681,P＜0.01;IHC:r =0.196,P＜0.05).CXCR5-CXCL13蛋白表达与肿瘤的淋巴结转移、远处转移、肿瘤分期及复发相关;在有淋巴结转移、有远处转移、中晚期患者及出现复发的患者中阳性率都明显较高(P＜0.05).此外,CXCL13阳性表达与结直肠癌的组织分化程度相关,分化越差组阳性率越高(P＜0.05).CXCR5-CXCL13表达与其他临床病理特征无关(P＞0.05).CXCR5及CXCL13阳性表达患者的5年复发率和5年生存率明显差于其阴性表达的患者(5年复发率:CXCR5:48.6％比14.8％,CXCL13:41.5％比22.7％;5年生存率:CXCR5:55.6％比91.4％,CXCL13:61.5％比84.1％)(P＜0.05);CXCR5及CXCL13阳性表达患者的中位复发时间和中位生存时间明显短于其阴性表达的患者[中位复发时间:CXCR5 (13.0±1.3)个月比(45.0±7.8)个月,CXCL13(13.0±1.3)个月比(29.0±11.2)个月;中位生存时间:CXCR5(17.0±1.1)个月比(55.0±14.4)个月,CXCL13(17.0±1.9)个月比(25.0±11.2)个月](P＜0.05).结论 CXCR5及CXCL13在结直肠癌的发生、发展和转移、复发中可能起着重要的作用,可作为预测结直肠癌转移和复发的有价值指标.     

乳腺癌小鼠动物模型中白细胞介素-17的表达及其意义

目的 探讨小鼠乳腺癌动物模型中白细胞介素-17(IL-17)的表达及意义.方法 以MA782/5S28102及4T1细胞株建立两种乳腺癌动物模型.分别于接种后1周和4周采用Western blot检测肿瘤组织中IL-17的表达.使用PMA+CD3单抗+CD28单抗刺激后,采用酶联免疫吸附试验(ELISA)检测肿瘤细胞和淋巴细胞培养体系上清中IL-17的含量.同时观察IL-17对培养体系及4T1荷瘤小鼠中肿瘤细胞生长的影响.结果 乳腺癌模型中晚期肿瘤组织中IL-17的表达水平均明显较早期有所升高.分离的肿瘤细胞接受刺激后,几乎不分泌IL-17,淋巴细胞分泌大量IL-17(P＜0.01).IL-17不能促进4T1细胞的生长(增长率分别为1.11±0.11和1.28 ±0.21,P＞0.05);将IL-17输注至4T1荷瘤小鼠的体内,可见肿瘤生长速度明显加快(P＜0.05).输注IL-17的荷瘤小鼠肿瘤组织中微血管密度(MVD)明显增加(MVD分别为:35.79±9.49,13.52±3.55,P＜0.01).结论 IL-17在晚期肿瘤组织中明显升高,IL-17可能通过促进肿瘤组织内微血管形成加快肿瘤的生长.

Abstract：

Objective To explore the impact of interleukin (IL) -17 expression on tumor growth in experimental models of murine mammary carcinoma and potential mechanisms. Methods Two murine cell lines, MA782/5S28102 and 4T1 were used to establish experimental models of murine mammary carcinoma. The IL-17 expression in tumor tissues derived from MA782-bearing mice or 4T1-bearing mice was detected in early and late stages of the tumor by Western blotting. The tumor cells and tumor-infiltrated-lymphocytes were separated from tumor tissues and cultured for 5 days with stimulation of PMA, anti-CD3 antibody and anti-CD28 antibody. The supernatants of culture media of stimulated tumor cells or tumor-infiltrated-lymphocytes were harvested and tested for IL-17 concentration by enzyme linked immunosorbent assay (ELISA). To evaluate the effect of IL-17 on the proliferation of tumor cells, 4T1 cells were culture in media with or without IL-17 and the cell number was counted on the day 5. For ire vivo assay, 4T1-bearing mice were injected with IL-17 or culture media via tail vein, and the tumor volume was measured. To assay the angiogenesis, the tumor tissues from 4T1-bearing mice with or without injection of IL-17 were stained with anti-CD31 antibody by immunohistochemistry. Results The IL-17 expression was significantly higher in late stage than in early stage of tumor in two experimental models. The tumor expression of IL-17 was secreted by tumor infiltrated lymphocytes (P ＜0.01). IL-17 could not increase the generation of tumor cells in vitro (1. 11 ±0. 11, 1. 28 ±0. 21 ,P ＞0. 05). But IL-17, injected into 4T1 -bearing mice, markedly enhanced in vivo tumor growth and significantly increased tumor vascularity (35. 79 ±9. 49, 13. 52 ±3. 55,P ＜0.01). Conclusion IL-17 in tumor tissue probably promotes tumor growth through enhancing angiogenesis.     

骨髓移植小鼠急性移植物抗宿主病早期弥漫性肺损伤中TH17细胞的作用

目的 探讨骨髓移植小鼠急性移植物抗宿主病(aGVHD)早期肺损伤中TH 17细胞的作用和机理.方法 Balb/c小鼠为受鼠,经致死量全身照射(TBI)后,输注C57BL/6小鼠来源的骨髓细胞和脾细胞,建立aGVHD模型.实验分为3组:TBI组小鼠仅接受TBI,异基因骨髓移植(BMT)组小鼠TBI后输注供者骨髓细胞和脾细胞,常山酮(HF)组小鼠TBI后输注骨髓细胞和脾细胞,并注射HF.动态观察小鼠GVHD的表现,并进行肺组织病理学、T淋巴细胞亚群及相关细胞因子的检测.结果 移植后小鼠出现典型GVHD的表现.移植后6d时HF组肺组织病理学评分为(2.00±0.35)分,BMT组为(0.67±0.07)分.BMT组TH 1细胞占CD4+T淋巴细胞的比例为(5.53±0.11)％,TH 17细胞占(1.04±0.34)％;HF组TH1细胞占(8.61±0.21)％,TH 17细胞占(0.49±0.07)％;组间比较,差异有统计学意义(P＜0.05).两组均未检测到TH2细胞.移植后6d,BMT组白细胞介素(IL)-17A为(2.81±0.19)pg/ml,γ干扰素(IFN-γ)为(42.97±0.23) pg/ml; HF组IL-17A＜0.8 pg/ml,IFN-γ为(9.89±0.51)pg/ml;组间比较,差异有统计学意义(P＜0.05).两组均未检测到IL-10.结论 在异基因造血干细胞移植早期阻断TH17细胞及其细胞因子的分泌,导致炎症因子分泌失衡,加重肺损伤.     

血浆外泌体miR-17-5p和miR-21对乳腺癌的诊断价值

目的探讨微小RNA-21（miR-21）和miR-17-5p在乳腺癌患者血浆外泌体中的表达水平及其诊断价值。 方法选取2017年6月至2018年3月于成都市第七人民医院就诊的86例乳腺癌患者为乳腺癌组,选取同期体检健康女性45例为对照组。采用实时定量聚合酶链反应（qRT-PCR）检测miR-21、miR-17-5p在两组血浆外泌体中的表达水平。根据qRT-PCR检测结果将乳腺癌患者分为miR-17-5p高表达组及低表达组,miR-21高表达组及低表达组,比较分析其与乳腺癌患者临床病理参数的关系。采用受试者工作特征曲线（ROC）分析血浆外泌体miR-21、miR-17-5p对乳腺癌的诊断价值。 结果乳腺癌组患者血浆外泌体miR-17-5p表达水平显著低于对照组（P<0.05）,而miR-21表达水平显著高于对照组（P<0.05）;miR-17-5p单独检测时曲线下面积（AUC）为0.677,敏感度为58.14%,特异度为75.56%,截断值为0.72;miR-21单独检测时AUC为0.694,敏感度为59.30%,特异度为77.78%,截断值为1.68;联合检测时敏感度为96.51%,特异度为95.56%,准确性为96.18%;联合检测诊断乳腺癌的敏感度、特异度及准确性均显著高于单项检测（P<0.05）。血浆外泌体miR-17-5p、miR-21表达水平均与TNM分期、分化程度、淋巴结转移、cerbB-2及Ki-67有关（P<0.05）。 结论血浆外泌体低表达的miR-17-5p与高表达的miR-21均可作为诊断乳腺癌的潜在生物学标志物。     

The effect of 5 alpha-androstane-3 alpha, 17 beta-diol and 17 beta-estradiol on the adult and immature chacma baboon prostate

We have studied the Chacma baboon prostate in an attempt to develop a primate model of benign prostatic hyperplasia. Anatomically, the baboon prostate can be divided into caudal, cranial, and prostatic urethral segments. A peri-urethral group of glands has been identified in the prostatic urethra. Following treatment with either 5 alpha-androstane-3 alpha, 17 beta-diol or 17 beta-estradiol, or the hormones in combination, the mature baboon prostate showed very little response by gravimetric or morphometric analysis. In contrast, the stimulatory effect of 5 alpha-androstane-3 alpha, 17 beta-diol on the caudal lobe of the immature baboon prostate and the prostatic urethral segment (a structure that is largely fibromuscular) was potentiated by the addition of 17 beta-estradiol. The weight of the immature baboon cranial prostate was increased by 5 alpha-androstane-3 alpha, 17 beta-diol treatment, but 17 beta estradiol did not potentiate androgen-induced growth. By morphometric analysis it could be shown that both the epithelial and stromal component of the immature baboon caudal prostate responded to 5 alpha-androstane-3 alpha, 17 beta-diol (androstanediol) treatment and that the addition of 17 beta-estradiol had a slight, but significant, potentiating effect on the androstanediol-induced increase of epithelial volume.     

寻常型白癜风患者外周血IL-17mRNA的检测及其临床意义

目的：探讨IL-17mRNA在寻常型白癜风患者外周血中的表达及其临床意义。方法：采用荧光实时定量RT-PCR方法对21例进展期白癜风患者、23例稳定期白癜风患者及30例健康对照外周血IL-17mRNA含量进行检测,并分析其表达水平与疾病病程与皮损面积的相关性。结果：进展期白癜风患者外周血IL-17mRNA的水平与健康对照组相比显著升高（P〈0.05）,稳定期白癜风患者IL-17mRNA的水平与健康对照组相比差异无统计学意义（P〉0.05）。白癜风患者IL-17mRNA的含量与病程无相关性（r=0.15,P〉0.05）,与皮损面积呈正相关（r=0.54,P〈0.05）。结论：IL-17在白癜风发病过程中可能发挥一定的作用。     

1,25(OH)2D3体外抑制小鼠Th17细胞分化的用研究

目的 探讨1,25(OH)2D3对Th17细胞分化的体外抑制作用.方法 通过对分离出的脾淋巴细胞进行CD4+T细胞分选,将不同浓度的1,25(OH)2D3加入到CD4+T细胞中并在诱导因子的作用下诱导其分化.通过ELISA检测培养上清中IL-17A和IL-22的浓度;流式细胞仪分析Th17细胞的比例及RT-PCR检测Th17细胞分化的转录因子的表达.结果 培养上清ELISA检测显示:与对照组相比,1,25(OH)2D3组的IL-17A和IL-22浓度随着加入1,25(OH)2D3浓度的增大而呈现逐渐降低的现象,差异且具有统计学意义(P＜0.01);流式结果显示:诱导分化后对照组Th17细胞比例最多,1,25(OH)2D3组处理后Th17细胞比例降低,且呈剂量依赖性;RT-PCR检测显示:与对照组相比,1,25(OH)2D3组IL-17A、IL-22,RORγt和RORα 表达量随着剂量的增加而逐渐降低,并具有统计学意义(P＜ 0.01).结论 体外实验表明,1,25(OH)2D3具有抑制Th17细胞分化的作用,表现为Th17细胞比例、分泌的细胞因子及特异的转录因子表达均减少.